J. Wesley Maddox

ORCID: 0000-0002-1630-2746
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About
Contact & Profiles
Research Areas
  • Retinal Development and Disorders
  • Neuroscience and Neuropharmacology Research
  • Neurobiology and Insect Physiology Research
  • Photoreceptor and optogenetics research
  • bioluminescence and chemiluminescence research
  • Ion channel regulation and function
  • CRISPR and Genetic Engineering
  • Erythrocyte Function and Pathophysiology
  • Ion Channels and Receptors
  • Neuroscience and Neural Engineering
  • Neuroinflammation and Neurodegeneration Mechanisms

The University of Texas at Austin
2022-2024

National Institute of Neurological Disorders and Stroke
2024

National Institutes of Health
2024

McPherson College
2024

Smith-Kettlewell Eye Research Institute
2024

University of Wisconsin–Madison
2024

Northwestern University
2024

University of Iowa
2020

Louisiana State University
2017

Synapses are fundamental information processing units that rely on voltage-gated Ca 2+ (Ca v ) channels to trigger -dependent neurotransmitter release. also play -independent roles in other biological contexts, but whether they do so axon terminals is unknown. Here, we addressed this unknown with respect the requirement for 1.4 L-type formation of rod photoreceptor synapses retina. Using a mouse strain expressing non-conducting mutant form 1.4, report protein, not its conductance, required...

10.7554/elife.62184 article EN cc-by eLife 2020-09-17

The sense of touch is crucial for cognitive, emotional, and social development relies on mechanically activated (MA) ion channels that transduce force into an electrical signal. Despite advances in the molecular characterization these channels, physiological factors control their activity are poorly understood. Here, we used behavioral assays, electrophysiological recordings, various mouse strains (males females analyzed separately) to investigate role calmodulin-like Ca 2+ sensor,...

10.1523/jneurosci.1402-23.2023 article EN Journal of Neuroscience 2024-01-23

C1QL1 is expressed in a subset of cells the brain and likely has pleiotropic functions, including regulation neuron‐to‐neuron synapses. Research progress on C1QL proteins been slowed by dearth available antibodies. Therefore, we created novel knock‐in mouse line which an HA‐tag inserted into endogenous C1ql1 locus. We examined entire brain, identifying previously unappreciated nuclei expressing C1QL1, presumably neurons. By total numbers, however, large majority C1QL1‐expressing are...

10.1002/1873-3468.14946 article EN FEBS Letters 2024-06-10

Retinal amacrine cells express nitric oxide (NO) synthase and produce NO, making NO available to regulate the function of cells. Here we test hypothesis that can alter GABAergic synaptic output We investigate this using whole cell voltage clamp recordings Ca2+ imaging cultured chick retinal When recording from receiving input other cells, find increases spontaneous postsynaptic current (sPSC) frequency. This increase in sPSC frequency does not require canonical receptor, soluble guanylate...

10.1152/jn.00803.2016 article EN Journal of Neurophysiology 2017-01-05

GABAergic signaling from amacrine cells (ACs) is a fundamental aspect of visual signal processing in the inner retina. We have previously shown that nitric oxide (NO) can elicit release GABA independently activation voltage-gated Ca2+ channels cultured retinal ACs. This voltage-independent quantal relies on influx mechanism with pharmacological characteristics consistent involvement transient receptor potential canonical (TRPC) TRPC4 and/or TRPC5. To determine identity these channels, we...

10.1152/jn.00500.2017 article EN Journal of Neurophysiology 2017-10-05

γ-Amino butyric acid (GABA) and glycine typically mediate synaptic inhibition because their ligand-gated ion channels support the influx of Cl − . However, electrochemical gradient for across postsynaptic plasma membrane determines voltage response cell. Typically, low cytosolic levels inhibition, whereas higher can suppress or promote depolarization. We previously reported that nitric oxide (NO) releases from acidic organelles transiently elevates , making to GABA excitatory. In this study,...

10.1152/jn.00511.2017 article EN Journal of Neurophysiology 2017-08-24

In congenital stationary night blindness, type 2 (CSNB2)—a disorder involving the Ca v 1.4 (L-type) 2+ channel—visual impairment is mild considering that mediates synaptic release from rod and cone photoreceptors. Here, we addressed this conundrum using a knockout (KO) mouse knock-in (G369i KI) expressing non-conducting 1.4. Surprisingly, 3 (T-type) currents were detected in cones of G369i KI mice KO but not wild-type mouse, ground squirrels, macaque retina. Whereas are blind, exhibit normal...

10.7554/elife.94908 article EN cc-by eLife 2024-02-02

In congenital stationary night blindness, type 2 (CSNB2)—a disorder involving the Ca v 1.4 (L-type) 2+ channel—visual impairment is mild considering that mediates synaptic release from rod and cone photoreceptors. Here, we addressed this conundrum using a knockout (KO) mouse knock-in (G369i KI) expressing non-conducting 1.4. Surprisingly, 3 (T-type) currents were detected in cones of G369i KI mice KO but not wild-type mouse, ground squirrels, macaque retina. Whereas are blind, exhibit normal...

10.7554/elife.94908.4 article EN cc-by eLife 2024-11-12

Voltage-gated Cav1 and Cav2 Ca2+ channels are comprised of a pore-forming α1 subunit (Cav1.1-1.4, Cav2.1-2.3) auxiliary β (β1-4) α2δ (α2δ-1-4) subunits. The properties these vary with distinct combinations Cav subunits alternative splicing the encoding transcripts. Therefore, impact disease-causing mutations affecting may depend on identities splice variants. Here, we analyzed effects congenital stationary night blindness type 2 (CSNB2)-causing mutation, I745T (IT), in Cav1.4 typical those...

10.1074/jbc.ra120.014138 article EN cc-by Journal of Biological Chemistry 2020-10-09

In congenital stationary night blindness type 2 (CSNB2)—a disorder involving dysfunction of the Ca v 1.4 2+ channel—visual impairment is relatively mild considering that mediates synaptic transmission by rod and cone photoreceptors. Here, we addressed this conundrum using a knockout (KO) mouse knock-in (KI) expressing non-conducting mutant. Surprisingly, aberrant 3 currents were detected in cones KI KO but not wild-type mice. Cone synapses, which fail to develop mice, are present enlarged...

10.7554/elife.94908.1 preprint EN 2024-02-02

In congenital stationary night blindness type 2 (CSNB2)—a disorder involving the Ca v 1.4 (L-type) 2+ channel—visual impairment is mild considering that mediates synaptic release from rod and cone photoreceptors. Here, we addressed this conundrum using a knockout (KO) mouse knock-in (G369i KI) expressing non-conducting 1.4. Surprisingly, 3 (T-type) currents were detected in cones of G369i KI mice KO but not wild-type mouse, ground squirrel, macaque retina. Whereas are blind, exhibit normal...

10.7554/elife.94908.2 preprint EN 2024-08-07

In congenital stationary night blindness type 2 (CSNB2)—a disorder involving the Ca v 1.4 (L-type) 2+ channel—visual impairment is mild considering that mediates synaptic release from rod and cone photoreceptors. Here, we addressed this conundrum using a knockout (KO) mouse knock-in (G369i KI) expressing non-conducting 1.4. Surprisingly, 3 (T-type) currents were detected in cones of G369i KI mice KO but not wild-type mouse, ground squirrel, macaque retina. Whereas are blind, exhibit normal...

10.7554/elife.94908.3 preprint EN 2024-08-28
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